Secrets to normal blood sugars audio series book from Dr. Richard Bernstein

Chapter 12: Weight Loss--If You're Overweight / Read It Online!

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Weight loss can significantly reduce your insulin resistance. You may recall from Chapter 1 that obesity, specifically abdominal (truncal, or visceral) obesity, causes insulin resistance and thereby can play a major role in the development of both impaired glucose tolerance and Type II diabetes. If you have this kind of obesity, it is important that weight loss become a goal of your treatment plan. Weight reduction can also slow down the process of beta-cell burnout by making your tissues more sensitive to the insulin you still produce, allowing you to require (and therefore produce or inject) less insulin.

It may even be possible, under certain circumstances, to completely reverse your glucose intolerance. Long before I studied medicine, I had a friend, Howie, who gained about 100 pounds over the course of a few years. He developed Type II diabetes and had to take a large amount of insulin (100 units daily) to keep it under control. His physician pointed out to him the likely connection between his diabetes and his obesity. To my amazement, during the following year, he was able to lose 100 pounds. At the end of the year, he had normal glucose tolerance, no need for insulin, and a new wardrobe. This kind of success may only be possible if the diabetes is of short duration, but it is certainly worth keeping in mind�weight loss can sometimes work miracles.

Before we talk about weight loss, it makes sense to talk about obesity.

The Thrifty Genotype

When I see a very overweight person, I don't think, "He ought to control his eating." I think, "He has the thrifty genotype."

What is the thrifty genotype?

The hypothesis for the thrifty genotype was first proposed by James V. Neel in 1962 to explain the high incidence of obesity and Type II diabetes among the Pima Indians of the southwestern United States. Evidence for a genetic determinant of obesity has increased over the years. Photographs of the Pimas from a century ago show a lean and wiry people. They did not know what obesity was and in fact had no word in their vocabulary to identify it.

Their food supply diminished in the early part of this century, something that had occurred repeatedly throughout their history. Now, however, they weren't faced with famine. The Bureau of Indian Affairs took over feeding them, and an astonishing thing happened. These lean and wiry people developed an astronomical incidence of obesity�100% of adult Pima Indians today are grossly obese, with a staggering rate of diabetes. Fully 60 percent of adults are Type II diabetics.

What happened to the Pimas? How did such apparently hardy and fit people become so grossly obese? Though their society was at least in part agrarian, they lived in the desert, where drought was frequent and harvests could easily fail. During periods of famine, those of their forebears whose bodies were not thrifty or capable of storing enough energy to survive without food died out. Those who survived were those who somehow could survive without food. How did they do it? Although it may be simplifying somewhat, the mechanism essentially works like this: Those who naturally craved carbohydrate and consumed it whenever it was available, even if they weren't hungry, would have made more insulin and thereby stored more fat. Add to this the additional mechanism of the high insulin levels caused by inherited insulin resistance, and serum insulin levels would have become great enough to induce fat storage sufficient to enable them to live through famines. (See Figure 1-1.) Truly survival of the fittest�provided famines would continue.

A strain of chronically obese mice created in the early fifties demonstrates quite vividly how valuable thrifty genes can be in famine. When these mice are allowed an unlimited food supply, they balloon and add as much as half again the body weight of normal mice. Yet deprived of food, these mice can survive a mind-boggling 40 days, versus 7�10 days for normal mice.

Recent research on these chronically obese mice provides some tantalizingly direct evidence of the effect a thrifty genotype can have upon physiology. In ordinary mice, a hormone called leptin is produced in the fat cells (also a hormone the human body produces, with apparently similar effect). The hormone tends to inhibit overeating, speed metabolism, and act as a modulator of level of body fat. A genetic "flaw" causes the obese mice to make a less effective form of leptin. In recent experiments, when injected with the real thing they almost instantly slimmed down. Not only did they eat less but they lost as much as 40 percent of their body weight, their metabolism sped up, and they became much more active. Many were diabetic, but their loss of weight (and the change in the ratio of fat to lean body mass) reversed or even "cured" their diabetes. Ordinary mice injected with leptin also ate less, became more active, and lost weight, though not as high a percentage. Research on humans has not advanced sufficiently to provide conclusive evidence that the mechanism is the same in obese humans, but researchers believe it is at least equivalent and probably related to more than one gene, and to different gene clusters in different populations.

In a full-blown famine, the Pima Indian's ability to survive long enough to find food is nothing short of a blessing. But when satisfying carbohydrate craving is suddenly just a matter of going to the grocery, what was once an asset becomes a very serious liability.

Although about 30 percent of the overall population of the United States is chronically obese, there is considerable reason to be concerned, because the number has been increasing by 1 percent each year. Some researchers attribute rising obesity in the United States at least in part to increasing numbers of former smokers. Others attribute it to the recent increase in carbohydrate consumption by those trying to avoid dietary fat. Whatever the reasons, obesity can lead to diabetes.

The thrifty genotype has its most dramatic appearance in isolated populations like the Pimas, which have recently been exposed to an unlimited food supply after millennia of intermittent famine. The Fiji Islanders, for example, were another lean, wiry people, accustomed to the rigors of paddling out against the Pacific to fish. Their diet, high in protein and low in carbohydrate, suited them perfectly. After the onset of the tourist economy that followed World War II, their diet changed to our high-carbohydrate western diet, and they too began (and continue) to suffer from a high incidence of obesity and Type II diabetes. The same is true of the Australian Aborigines after the Aboriginal Service began to provide them with grain. Ditto for South African blacks who migrated from the bush into the big cities. Interestingly, a study that paid obese, diabetic South African blacks to go back to the countryside and return to their traditional high-protein, low-carbohydrate diet found that they experienced dramatic weight loss and regression of their diabetes.

It's clear that thrifty genotypes work in isolated populations to make metabolism supremely energy-efficient, but what happens when the populations have unrestricted access to high-carbohydrate foods?

It would appear that the mechanism of the thrifty genotype works something like this: Certain areas of the brain associated with satiety�that sensation of being physically and emotionally satisfied�have lower levels of certain chemicals known as neurotransmitters. A number of years ago, Drs. Richard and Judith Wurtman at the Massachusetts Institute of Technology (MIT) discovered that the level of the neurotransmitter serotonin is raised in certain parts of the hypothalamus of the animal brain when the animal eats carbohydrate, especially fast-acting concentrated carbohydrate like bread. Serotonin is a neurotransmitter that seems to reduce anxiety as it produces satiety. Other neurotransmitters such as dopamine and norepinephrine can also affect our senses of satiety and anxiety, euphoria and dysphoria. There are now seventy-five known neurotransmitters, and many more of them may affect mood and food in ways that are just beginning to be researched and understood.

In persons with the thrifty genotype, deficiencies of these neurotransmitters (or diminished sensitivity to them in the brain) causes both a feeling of hunger and a mild dysphoria�often a sensation of anxiety, and the opposite of euphoria. Eating carbohydrates temporarily causes the individual to feel not only less hungry but also more at ease.

A frequent television sitcom scenario is the woman just dumped by her boyfriend who plops down on the couch with a pie or half a gallon of ice cream, a spoon, and the intention of eating the whole thing. She's not really hungry. She's depressed and trying to make herself feel better. She's indulging herself, we think, rewarding herself in a way for enduring one of life's traumas, and we laugh because we understand the feeling. But there is a very real biochemical mechanism at work here. She craves the sugar in the pie or the ice cream not because she's hungry but because she knows, consciously or not, that it really will make her feel better. Contrary to popular belief, the fat in the ice cream or in the crust of the pie doesn't make much of a difference. It's the carbohydrate that will increase the level of certain neurotransmitters in her brain and make her feel better temporarily. The side effect of the carbohydrate is that it also causes her blood sugar to rise and her body to make more insulin; and, as she sits on the couch, the elevation in her insulin will turn the sugar she eats into fat.

On television the actress never gets fat. But for the real-life woman, high serum insulin levels from eating high-carbohydrate foods will cause her to crave carbohydrate again. If she is a Type I diabetic making no insulin, she'll have to inject a lot of insulin to get her blood sugar down, with the same effect�more carbohydrate craving and building up of fat reserves.

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